Pubmed du 29/12/24
1. Almalki AH, Bamaga AK, Alharbi A, Abduljabbar MH, Alnemari RM, Baali FH, Algarni MA, Ahmed MF, Ramzy S. Exploring the association between serum magnesium level and autism spectrum disorder using validated spectrofluorimetric method. Anal Biochem. 2024; 699: 115755.
Magnesium is an essential mineral in biological systems and has a significant impact on brain health. Its deficiency has been found to correlate with irregular metabolic processes and neurodevelopmental disorders. The objective of this research was to establish and validate an analytical approach based on the standard addition methodology for determining endogenous magnesium levels in the serum of autistic and healthy children. Analytically, the approach involved functionalizing fluorescent graphene quantum dots with a magnesium-phosphomolybdic acid ion pair complex, followed by measuring magnesium-induced fluorescence quenching on the functionalized graphene quantum dots, which is concentration-dependent. The approach was validated in accordance with the ICH M10 requirements for bioanalytical technique validation, and it reliably quantified magnesium concentrations in the serum of both autistic and healthy children. The study found that autistic children have considerably lower serum magnesium concentrations than healthy children (P < 0.01), indicating a correlation between magnesium deficiency and autism spectrum disorder. The average serum magnesium levels (mg/dl) recorded for the autistic and healthy groups were 2.03 ± 0.33 and 2.28 ± 0.26, respectively.
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2. Basra M, Miceli L, Mundra V, Stern-Harbutte A, Patel H, Haynes J, Parmar MS. Exploring the neurotoxic effects of microbial metabolites: A potential link between p-Cresol and autism spectrum disorders?. Brain Res. 2024: 149427.
Autism spectrum disorder (ASD) is a neurodevelopmental disorder with a complex etiology, including genetic and environmental factors. A growing body of evidence (preclinical and clinical studies) implicates a potential role of gut microbiome dysregulation in ASD pathophysiology. This review focuses on the microbial metabolite p-Cresol, produced by certain gut bacteria such as Clostridium, and its potential role in ASD. The review summarizes studies investigating the gut microbiome composition in ASD patients, particularly the increased abundance of Clostridium species and associated gastrointestinal symptoms. The potential neurotoxic effects of p-Cresol are explored, including its influence on neurotransmitter metabolism (especially dopamine), neuroinflammation, and brain development. The mechanistic findings from the preclinical studies of p-Cresol’s induction of ASD-like behaviors and its impact on the dopaminergic system are discussed. Literature studies indicated increased levels of p-Cresol in the urine of patients with ASD. This increasing evidence suggests that p-Cresol may serve as a crucial biomarker for understanding the relationship between gut microbiota and ASD, opening avenues for potential diagnostic and therapeutic interventions.
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3. Cao C, Li J, Cui W, Dai J, Guan Z, Wang D, Zhao X. Metalomics Revealed that Changes of Serum Elements were Associated with Oxidative Stress-Induced Inflammation of Cortex in a Mouse Model of Autism. Biol Trace Elem Res. 2024.
Autism spectrum disorder (ASD) is a neurodevelopmental disorder emerging during early childhood. However, the mechanism underlying the pathogenesis of ASD remains unclear. This study investigated the alterations of elements in serum and prefrontal cortex of BTBR T + tf/J (BTBR) mice and potential mechanisms. The male BTBR mice were used for experimental group and C57BL/6 J (C57) mice were used for control group (n = 15). After behavioral tests were monitored, serum and prefrontal cortex of mice were analyzed by ICP-MS. The results demonstrated that the level of copper (Cu) was increased, and the levels of calcium (Ca), magnesium (Mg), selenium (Se), cobalt (Co), iron (Fe) and zinc (Zn) were decreased in BTBR mice compared to C57 mice (p < 0.01). The levels of above differential elements in serum demonstrated positive correlations with those in prefrontal cortex. Meanwhile, differential elements in prefrontal cortex had correlations with the total distance traveled (open field test) and the number of marbles buried (marble burying test) in BTBR mice (p < 0.05 or p < 0.01). The abnormally changed elements in serum might cross blood-brain-barrier into the brain and lead to oxidative stress, causing inflammation. Furtherly, the levels of inflammation-related indicators including tumor necrosis factor-alpha (TNF-α), nuclear factor kappa-B (NF-κB), interleukin-6 (IL-6) and interleukin-1β (IL-1β) were increased in prefrontal cortex of BTBR mice (p < 0.01), which were consistent with the aforementioned results. Our study suggested that the abnormal elements in the serum of BTBR mice may cause oxidative stress and inflammation in prefrontal cortex, which might contribute to increase the understanding of ASD pathogenesis.
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4. Hsueh YP. Signaling in autism: Relevance to nutrients and sex. Curr Opin Neurobiol. 2024; 90: 102962.
Autism spectrum disorders (ASD) are substantially heterogeneous neuropsychiatric conditions with over a thousand associated genetic factors and various environmental influences, such as infection and nutrition. Additionally, males are four times more likely than females to be affected. This heterogeneity underscores the need to uncover common molecular features within ASD. Recent studies have revealed interactions among genetic predispositions, environmental factors, and sex that may be critical to ASD etiology. This review focuses on emerging evidence for the impact of nutrients-particularly zinc and amino acids-on ASD, as demonstrated in mouse models and human studies. These nutrients have been shown to influence synaptic signaling, dendritic spine formation, and behaviors linked to autism. Furthermore, sex-based differences in nutritional requirements, especially for zinc and amino acids, may contribute to the observed male bias in autism, indicating that interactions between nutrients and genetic factors could be integral to understanding and potentially mitigating ASD symptoms.
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5. Levy L, Ambaw A, Ben-Itzchak E, Holdengreber E. A real-time environmental translator for emotion recognition in autism spectrum disorder. Sci Rep. 2024; 14(1): 31527.
Autism spectrum disorder (ASD) involves challenges in communication and social interaction, including challenges in recognizing emotions. Existing technological solutions aim to improve social behaviors in individuals with ASD by providing learning aids. This paper presents a real-time environmental translator designed to enhance social behaviors in individuals with ASD using sensory substitution. Our system utilizes vibrotactile and visual feedback to interpret and convey emotional states through vibration patterns emitted from small vibration motors on the user’s temple, complemented by color-coded displays of emotional intensity. It can detect seven emotions: neutral, sad, happy, angry, disgust, surprise, and fear. Testing with adults with ASD showed they could adapt to the system in about 19 min, enabling them to intuitively and immediately recognize others’ emotions. This innovative approach presents a promising advancement in emotion recognition technology for individuals with ASD, offering potential benefits in enhancing their social interactions and communication skills.
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6. Liu H, Zhu X, Ge B, Huang M, Li X. The association between screen exposure and autism spectrum disorder in children: meta-analysis. Rev Environ Health. 2024.
INTRODUCTION: The goal is to provide light on the contentious relationship between screen exposure and childhood autism spectrum disorder (ASD). By conducting two meta-analyses that showed a potential association, including screen exposure effect by ASD and ASD risk by screen exposure, we aimed to clarify the potential causality between screen exposure and childhood ASD. CONTENT: The literature published up to December 2023 were systematically collected, and the combined effect values of weighted mean difference (WMD) and 95 % confidence interval (CI) and odds ratio (OR) and 95 % CI were calculated using two meta-analyses using the STATA 12.0. A total of 197,357 children, including 4,599 childhood ASD, were finally included in 10 studies. The results showed that children with ASD had higher levels of screen time exposure than healthy controls (combined effect value WMD=0.27, 95 % CI: 0.12-0.41, p<0.001). An increased risk of ASD was also found in children with high screen exposure compared to the low screen exposure group (OR=1.5395 % CI: 1.14-2.06). SUMMARY AND OUTLOOK: The development of childhood ASD may be associated with screen exposure. Future prospective studies are needed to verify the relationship between screen exposure and ASD in children.
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7. Tanabe M, Saito Y, Takasaki A, Nakano K, Yamamoto S, Suzuki C, Kawamura N, Hattori A, Oikawa M, Nagashima S, Yanagi S, Yamaguchi T, Fukuda T. Role of immature choroid plexus in the pathology of model mice and human iPSC-derived organoids with autism spectrum disorder. Cell Rep. 2024; 44(1): 115133.
During gestation, the choroid plexus (ChP) produces protein-rich cerebrospinal fluid and matures prior to brain development. It is assumed that ChP dysfunction has a profound effect on developmental neuropsychiatric disorders, such as autism spectrum disorder (ASD). However, the mechanisms linking immature ChP to the onset of ASD remain unclear. Here, we find that ChP-specific CAMDI-knockout mice develop an immature ChP alongside decreased multiciliogenesis and expression of differentiation marker genes following disruption of the cerebrospinal fluid barrier. These mice exhibit ASD-like behaviors, including anxiety and impaired socialization. Additionally, the administration of metformin, an FDA-approved drug, before the social critical period achieves ChP maturation and restores social behaviors. Furthermore, both the ASD model mice and organoids derived from patients with ASD developed an immature ChP. These results propose the involvement of an immature ChP in the pathogenesis of ASD and suggest the targeting of functional maturation of the ChP as a therapeutic strategy for ASD.
